General Cascade of Disorders
Any comatose state begins with an extreme stressor that triggers a universal pathological cascade. First and foremost, the brain suffers maximal damage, followed by the functional failure of other organ systems.
Key pathogenetic links include:
- Hypoxia and cellular energy depletion.
- Intoxication (accumulation of endogenous or exogenous toxins).
- Acid-base imbalances (predominantly persistent acidosis).
- Dysionia and dyshydration (fluid and electrolyte balance failure).
- Dysbalance of biologically active substances (hormones, neurotransmitters, cytokines).
In the early stages of coma, specific symptoms depend on the underlying etiology. However, as the condition worsens, the clinical picture becomes universal: physiological systems collapse, regulation regresses to a primitive tissue level, and multi-organ failure ensues. Alveolar ventilation drops in the lungs, blood viscosity changes and triggers disseminated intravascular coagulation (DIC), while digestion halts in the gut, leading to autoinfection.
Energy Crisis and Cerebral Edema
Neurons are critically dependent on oxygen. When cerebral blood flow ceases, events unfold rapidly:
- Within 8–10 seconds, acute oxygen deficit develops, cellular energy drops, and complete loss of consciousness occurs.
- Within 4–7 minutes, glucose reserves are exhausted. Escalating intracellular acidosis blocks even anaerobic metabolism, and ATP reserves are irreversibly depleted.
Without energy, neurons cannot maintain ion pump function. Sodium (Na⁺) rapidly accumulates inside cells, sharply increasing osmotic and oncotic pressure. Water rushes from blood vessels into neurons and the interstitium, causing cerebral edema and brain swelling. Morphologically, this is accompanied by venous hyperemia and petechial hemorrhages in the nervous tissue.
Toxic Shock and Electrogenesis Failure
Coma is invariably accompanied by severe intoxication. Toxins target neurons, the heart, blood cells, and endocrine glands. A vicious cycle is established: toxins damage the liver and kidneys, further impairing detoxification and waste clearance.
For example, in hepatic coma, bowel-derived protein breakdown products (putrescine, cadaverine, phenol and indole derivatives) as well as ammonia accumulate in the blood. Excess ammonia inhibits enzymes and impairs GABA/benzodiazepine receptor function.
Concurrently, dysionia develops—an electrolyte imbalance that disrupts normal tissue electrogenesis:
- The formation of resting membrane potentials and action potentials is distorted.
- The excitability of nervous and muscle tissue declines.
- Severe cardiac rhythm disturbances (up to ventricular fibrillation) and respiratory disorders emerge.
Specific Features of Certain Coma Types
| Coma Type | Key Mechanisms and Clinical Manifestations |
|---|---|
| Post-traumatic | A consequence of severe concussion, contusion, and cerebral edema. Characterized by areflexia, paralysis, and seizures. Basilar skull fractures damage cranial nerves VII and VIII, presenting with "raccoon eyes" (periorbital ecchymosis), CSF otorrhea/rhinorrhea, and bleeding from the ears and nose. |
| Apoplectic | Occurs during a stroke (hemorrhagic or ischemic). Microvascular permeability increases sharply, and an ischemic "penumbra" forms around the core lesion. Associated with an extremely poor prognosis. |